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首页> 美国卫生研究院文献>American Journal of Physiology - Endocrinology and Metabolism >Using a novel coculture model to dissect the role of intramuscular lipid load on skeletal muscle insulin responsiveness under reduced estrogen conditions
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Using a novel coculture model to dissect the role of intramuscular lipid load on skeletal muscle insulin responsiveness under reduced estrogen conditions

机译：使用一种新型的共培养模型来剖析肌内脂质负荷在雌激素减少的条件下对骨骼肌胰岛素反应性的作用

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Reductions in estrogen function lead to adiposity and peripheral insulin resistance. Significant metabolic changes have been found in adipocytes and skeletal muscle with disruptions in the estrogen-signaling axis; however, it is unclear if intercellular communication exists between these tissues. The purpose of this study was to examine the impact of isolated adipocytes cocultured with single adult skeletal muscle fibers (SMF) collected from control female (SHAM) and ovariectomized female (OVX) mice. In addition, a second purpose was to compare differential effects of primary adipocytes from omental and inguinal adipose depots on SMF from these same groups. OVX SMF displayed greater lipid content, impaired insulin signaling, and lower insulin-induced glucose uptake compared with SHAM SMF without coculture. In the SHAM group, regardless of the adipose depot of origin, coculture induced greater intracellular lipid content compared with control SHAM SMF. The increased lipid in the SMF was associated with impaired insulin-induced glucose uptake when adipocytes were of omental, but not inguinal, origin. Coculture of OVX SMF with omental or inguinal adipocytes resulted in higher lipid content but no further reduction in insulin-induced glucose uptake compared with control OVX SMF. The data indicate that, in the OVX condition, there is a threshold for lipid accumulation in skeletal muscle beyond which there is no further impairment in insulin responsiveness. These results also demonstrate depot-specific effects of adipocyte exposure on skeletal muscle glucose uptake and further implicate a role for increased intracellular lipid storage in the pathogenesis of insulin resistance when estrogen levels are reduced.
机译：雌激素功能降低导致肥胖和外周胰岛素抵抗。在脂肪细胞和骨骼肌中发现了明显的代谢变化，雌激素信号转导受到破坏。然而，尚不清楚这些组织之间是否存在细胞间通讯。这项研究的目的是检查与从对照组雌性（SHAM）和卵巢切除雌性（OVX）小鼠收集的单个成年骨骼肌纤维（SMF）共培养的分离的脂肪细胞的影响。此外，第二个目的是比较来自网膜和腹股沟脂肪库的原代脂肪细胞对这些相同组的SMF的不同作用。与不进行共培养的SHAM SMF相比，OVX SMF显示出更高的脂质含量，受损的胰岛素信号传导和更低的胰岛素诱导的葡萄糖摄取。在SHAM组中，无论脂肪来源如何，与对照SHAM SMF相比，共培养诱导的细胞内脂质含量更高。当脂肪细胞起源于网膜而不是腹股沟时，SMF中脂质的增加与胰岛素诱导的葡萄糖摄取受损有关。与对照OVX SMF相比，OVX SMF与网膜或腹股沟脂肪细胞的共培养导致脂质含量更高，但胰岛素诱导的葡萄糖摄取没有进一步降低。数据表明，在OVX状态下，骨骼肌中存在脂质蓄积阈值，超过此阈值，胰岛素反应性将不再受到损害。这些结果还证明了脂肪细胞暴露对骨骼肌葡萄糖摄取的仓库特异性作用，并且当雌激素水平降低时，进一步暗示了细胞内脂质储存增加在胰岛素抵抗的发病机理中的作用。

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